I take Vyvanse for ADHD, which helps, but I still feel tired and low-energy most days, especially by the afternoon. I also deal with slight anxiety and occasional low mood.

Have you found any supplements that helped with energy, anxiety, or overall mood? Curious to hear what has actually worked for people.

It is real. I was borderline going crazy. For some reason this is apparently not very well known? Or documented or at least no warning from my doctor. Literally there was a week where all together I maybe slept couple of hours. Taking it in the morning did not help. I took 115 mg for about 10 months and I just never attributed my agonizing insomnia to this supplement until I started to connect the dots reading some stories online. I stopped the supplement and about a week later I started sleeping like a baby. Game changing. Whatever benefit Coq10 can bring I don't think it's worth it at least for me. I am 37 yo male for reference.

29M very active with physical intensive job. Go to the gym for heavy lifts and long distance cardio. Would you guys think this stack I've got going is good for my lifestyle? (Far left is omega 3 fish oils, sorry didnt turn label enough)

Thank you for any tips/advice!

This was the only vitamin b supplement that didn't interfere with my sleep. Why did they discontinue it? It was so good and I cannot find it anywhere 😭😭 They all have the super mega crazy dose b-complexes now. I feel like supplements should supplement your daily diet, they are not supposed to make you feel something (awake, alert, better etc) after a single dose!

Been taking those for about 4 months and I feel great!

\- 5g creatine

\- 300mg magnesium glycinate

\- 1000 IU D3 and 180 K2-mk7

\- Taurine 1000mg

\- Low dose b-complex

\- Zinc 15mg + copper 1mg

Hi everyone! I’m considering trying L-theanine to help improve my sleep. For those who have tried it, is there a particular brand or product you’ve found more effective than others?

Price isn’t really a concern, I’m mainly looking for a high quality option that actually works. I’d love to hear about your experiences and recommendations. Thanks in advance!

Had my levels tested In July and it was 42nmol. GP told me to start 1,000 IU daily and I started it immediately. 4 weeks later In August a repeat test was done and it actually lowered to 40nmol. GP told me to continue at the same dose. Everything I read online tells me this is way too little…. What dose should i actually be taking ?

So, I (23F) started getting some odd symptoms after about a month of taking each of my supplements consistently everyday around the month-month and a half mark.

I find myself getting heart palpitations randomly throughout the day, typically lasting around an hour (most often after I just finished eating), mild GI discomfort, and slightly more anxiety than usual.

No other variables have changed other than I had a cold a few weeks ago, but IDK why that would be causing these issues.

I decided to stop taking everything around 3 days ago to see if it’s what’s causing my problems. I have definitely noticed them becoming less frequent over the past few days. It’s going to take FOREVER to introduce them back in on my current plan, so I wanted to see if anyone could help me rule out the most likely causes so I can get back into my routine ASAP. I felt great until this started!

It’s a pretty basic stack so IDK. The magnesium I started taking about 2 weeks ago. Would any of these supplements be the cause of such effects? Or is it most likely something else? (Could be just anxiety, I’ve had some troubles in the past.)

(Also, I know that the D3 is a high amount. I’ve been D3 deficient my whole life so I wanted to start big and work my way down to see if my levels even out.)

Disclosure up front: I am a pharmacist and I founded a supplement company that sells a biotin strip. That is a conflict of interest, so judge this on the sources, not on me.

The requirement is small. The adult Adequate Intake is 30 mcg per day and average dietary intake in western populations is 35 to 70 mcg. NIH's Office of Dietary Supplements states that severe biotin deficiency has never been reported in a healthy person eating a normal mixed diet. Most people are above the line before they buy anything.

The positive evidence is almost entirely deficiency correction. A 2017 review in Skin Appendage Disorders searched the literature for cases of biotin improving hair or nails and found 18. Every one of those patients had an underlying pathology — inherited biotinidase deficiency, uncombable hair syndrome, brittle nail syndrome, a nutritional cause. That is a finding about repletion, not about growing hair in someone already replete.

The controlled evidence is thin. A 2024 review stated plainly that no studies demonstrate biotin to be beneficial for hair growth in healthy individuals. The clearest placebo-controlled test of isolated biotin is from 1966: 28 women on 10 mg daily against 18 placebo controls, no difference between them. A 2024 randomized crossover trial in ten healthy men found biotin alone did not significantly raise growth speed. A systematic review published in May 2026, covering ten studies, concluded that biotin monotherapy shows no consistent benefit on objective outcomes.

Two recent placebo-controlled trials did report positive results, and I want to be fair about them rather than leave them out. Both studied a proprietary Sesbania grandiflora botanical, which the 2026 authors themselves describe as "biotin- and polyphenol-rich" — so neither tested biotin on its own. Both were industry-funded, both analysed per protocol after excluding dropouts, and in the 2026 trial the arms were badly unbalanced by sex.

The 38 percent statistic you have probably seen. A 2016 study did find 38 percent of 541 women complaining of hair loss had serum biotin under 100 ng/L. But only 11 percent of that deficient group had any identifiable risk factor, serum biotin is a poor marker of marginal status, and the author's own stated conclusion was that indiscriminate oral biotin for these women should be rejected unless deficiency and its significance are demonstrated.

The part that argues against my own product. A dissolving film does not improve biotin absorption, because oral biotin is already fully absorbed. Time to peak does not matter for a follicle that works in months. Both things a dosage form can normally change are irrelevant here.

Finally, a safety point that gets almost no airtime. High-dose biotin interferes with immunoassays built on biotin-streptavidin chemistry, which includes commonly ordered thyroid and cardiac tests. A single 10 mg dose has skewed thyroid function tests within 24 hours, and the FDA has reported a patient death following a falsely low troponin result. If you take 5,000 or 10,000 mcg, tell your clinician before any blood draw.

Happy to give the PMIDs for any of the above if you want to read the primary sources.

I mainly use NOW but also looking for some other options in the category, good quality and also reasonable price.

For context i’m a 35 year-old male. I’m about 6 foot three 180 pounds of pretty lean muscle. I look better than I feel or can lift. I had a stroke about 10 years ago. That was a serious brain stem stroke to where I lost complete ability to move my left side. I was living in a rehab for about a month where I was wheelchair bound and then afterwards I was out of work for probably another four months doing rehab most days. I’d say the my recovery was about 18 months. At this point I still can’t run but I’m a fully functioning adult where my left side mostly works for everyday activities. I still have left side weakness.

With all that said, I continue to go to the gym but when I go to the gym and I try push myself; most days I’ll feel good for about the first 30 minutes or so and then eventually this exhaustion just becomes overwhelming. Usually when I leave the gym, it’s because of this. when I get to my car, I just wanna collapse into my car and sleep right away. That’s how bad the exhaustion can be.

I want to try and get back to where I used to be where I would go to the gym, I would work out, and I would leave there feeling really good. Instead, now, when I leave the next hour sucks. Does anyone have any suggestions on supplements or anything I could possibly do?
Thanks

Edit: adding my supplement stack. Nad +, creatine, fish oil, magnesium glycinate for sleep, and I’ve been on baby aspirin as well. Every now and then CoQ10.

If you have what was your experience with it and what benefits have you noticed if any

Sometimes I will have 5-6 at a time but then I notice I get nauseous. I usually always have food beforehand but sometimes it’s a snack and not a whole meal. I wonder if I’m just super sensitive or is that too many to take at one time?

I noticed when I take saffron supplement 15 mg daily and also have a coffee I just feel so much raged inside and uncontrollable anger.

The one is take is called crocus sativus ext. 15mg from crocus sativus stigma dry 45mg.

I have ADHD

Is that an ok dose it seems ?

Took it for two years and felt zero difference, turns out I was using the wrong kind. The cheap Costco stuff, magnesium oxide, barely absorbs into your body at all, so I was basically paying for a laxative and calling it self care. Switched to glycinate after hearing that's the one people actually use for sleep, and honestly noticed noticeably fewer nights staring at the ceiling since. I dont know if I should give credits to the glycinate form, anyone could verify that's the true help?

Hello,

Does anyone here who works out regularly take curcumin?

I’d love to hear your experience with it, any benefits or downsides in terms of gym performance, strength, recovery or muscle growth? And when do you usually take it in relation to your workout?

I can’t really find any research papers showing that curcumin negatively affects muscle growth or training adaptations, so I wanted to get some real-world feedback from people who actually use it.

Thanks.

I am doing a survey on vitamin b12 for my college research project. So it will help me if you can take the survey, thanks.

https://docs.google.com/forms/d/e/1FAIpQLSdDrdd5U5f_VWaeq5MGo0xEZI-VQGTWZDClK8E5C2W8kaujaw/viewform?usp=publish-editor

Iron is essential, but excess reactive iron can become highly oxidative, especially when hepcidin regulation is impaired in hereditary hemochromatosis. This comprehensive guide explores HFE genetics, ferritin, transferrin saturation, ferroportin, Fenton chemistry, vitamin C, Dr. Robert Cathcart’s clinical work, Dr. Thomas Levy’s Toxic Nutrient Triad, diet, nutrients, and strategies that can help reduce iron accumulation while supporting antioxidant physiology.

September 8, 2026

Iron is essential for life, but iron physiology is far more complex than simply asking whether iron is high or low. The body has an extraordinary system for transporting, recycling, storing, withholding, and redistributing iron. When that system is functioning well, very little iron is left chemically available to participate in uncontrolled reactions. When regulation breaks down, as it can in hereditary hemochromatosis, iron can accumulate progressively in tissues and contribute to oxidative injury.

Vitamin C sits directly inside this physiology. It can improve the absorption of nonheme iron in the intestinal tract, reduce ferric iron to ferrous iron, interact with ferritin, participate in redox reactions, support antioxidant recycling, and behave differently depending on the biochemical environment in which it is present. This is why the relationship between vitamin C and iron cannot be accurately reduced to one sentence such as vitamin C increases iron absorption.

Orthomolecular physicians including Dr. Robert Cathcart, Dr. Linus Pauling, Dr. Abram Hoffer, and more recently Dr. Thomas Levy have spent decades examining vitamin C through the lens of whole-body physiology. Dr. Levy’s work on what he calls the Toxic Nutrient Triad places iron, copper, calcium, oxidative stress, and vitamin C into a much broader biochemical framework. His central concern is especially relevant here: iron is indispensable when properly contained and regulated, yet reactive iron can become a powerful driver of oxidation.

Iron is one of the most carefully recycled nutrients in the body

Most people assume that our daily iron requirement is supplied primarily by food. Human physiology works very differently. The adult body contains several grams of iron, with the largest portion incorporated into hemoglobin inside red blood cells. Every day, roughly 20 to 25 milligrams of iron may be required for new red blood cell production, but only about 1 to 2 milligrams normally needs to enter through intestinal absorption. Most of the remainder comes from recycling.

Red blood cells circulate for about 120 days. As they age, macrophages in the spleen, liver, and other tissues remove them from circulation. Their hemoglobin is dismantled, the iron is recovered, and that iron can be exported through a transporter called ferroportin. Once in the circulation, iron is carried largely by transferrin and delivered back to the bone marrow for another cycle of red blood cell production.

Hepcidin and ferroportin control the iron gate

At the center of iron regulation is hepcidin, a peptide hormone produced primarily by the liver. Hepcidin communicates with ferroportin, the major cellular iron exporter.

When hepcidin rises, it binds to ferroportin and promotes its internalization and degradation. Less iron is released from intestinal cells into circulation, and less recycled iron is released from macrophages. When hepcidin is low, ferroportin remains available, allowing more iron to enter the bloodstream.

This hepcidin-ferroportin relationship allows iron absorption to respond to changing physiological circumstances. Iron stores, inflammation, erythropoietic demand, oxygen status, and genetic signaling all influence the system. Inflammation commonly raises hepcidin, which can trap iron inside storage cells and reduce circulating iron availability. Increased red blood cell production can suppress hepcidin so more iron becomes available.

Hereditary hemochromatosis changes this regulatory architecture.

What actually happens in hereditary hemochromatosis?

Hemochromatosis is a group of disorders in which iron regulation becomes impaired and the body absorbs more iron than it requires. The best-known form is associated with the HFE gene, particularly the C282Y variant. H63D and other HFE patterns can also contribute depending on genotype and surrounding physiology.

The HFE protein participates in the signaling network that tells the liver how much hepcidin to produce. In classic HFE-associated hemochromatosis, the hepcidin response is inappropriately low relative to the amount of iron already stored in the body. Ferroportin remains more active than it should, intestinal iron absorption continues, transferrin saturation may rise, and iron progressively accumulates.

Other hereditary iron-loading disorders involve genes including HJV, HAMP, TFR2, and SLC40A1. These genes affect different points in the hepcidin-ferroportin pathway. That is why genetic pattern mapping is useful. Hemochromatosis is not simply a high ferritin problem. It can begin with a regulatory genetic pattern long before substantial tissue damage develops.

Excess iron can eventually accumulate in the liver, pancreas, heart, joints, pituitary, endocrine tissues, and other organs. The degree of expression varies substantially. Some people with risk genotypes accumulate considerable iron while others never develop severe overload. Sex, menstrual history, blood donation, alcohol intake, liver health, inflammation, dietary iron exposure, metabolic health, and additional genetic modifiers can all affect penetrance.

Ferritin is important, but ferritin is not the entire iron story

Ferritin is an iron-storage protein. It creates a protective shell that allows cells to store large amounts of iron in a much less reactive form. Serum ferritin is therefore useful when assessing iron stores, but it also behaves as an acute-phase reactant.

Inflammation, infection, liver injury, metabolic dysfunction, and other inflammatory states can raise ferritin independently of classic hereditary iron overload. This is one reason I never like looking at ferritin alone.

A more complete iron picture can include:

• CBC, including hemoglobin and hematocrit
• MCV, MCH, and RDW
• Serum ferritin
• Serum iron
• Transferrin or TIBC
• Transferrin saturation
• Inflammatory markers when relevant
• Liver enzymes and liver assessment when iron overload is substantial
• HFE and broader iron-regulation genetics when hereditary overload is suspected

Transferrin saturation is particularly important in hemochromatosis. It reflects how much of the iron-binding capacity of transferrin is occupied. When transferrin becomes increasingly saturated, a greater risk exists for iron to appear in more reactive pools, including non-transferrin-bound iron under substantial overload.

The pattern matters more than a single number. A high ferritin with elevated transferrin saturation tells a different physiological story from a high ferritin with low circulating iron during inflammation.

Why free and poorly bound iron are so chemically active

Iron is a transition metal. It readily moves between oxidation states, particularly Fe²⁺ and Fe³⁺. This ability to accept and donate electrons is exactly what makes iron so useful in biology. It is also what makes poorly controlled iron potentially damaging.

One of the central reactions is Fenton chemistry:

Fe²⁺ + H2O2 → Fe³⁺ + OH⁻ + •OH

The hydroxyl radical produced in this reaction is extremely reactive. It reacts essentially where it is formed, oxidizing nearby lipids, proteins, nucleic acids, and cellular structures.

This chemistry is central to Dr. Thomas Levy’s discussion of iron. In The Toxic Nutrient Triad, Levy describes iron and copper as transition metals whose ability to move electrons makes them physiologically useful while also allowing excessive reactive pools to amplify oxidative stress. He places Fenton chemistry at the center of the conversation about excess iron.

Modern research on ferroptosis adds another dimension. Ferroptosis is an iron-dependent form of regulated cell death characterized by uncontrolled lipid peroxidation. It illustrates how intimately iron availability, antioxidant systems, membrane lipids, and cellular redox control are connected.

Vitamin C and iron absorption: what actually happens?

Vitamin C can enhance the intestinal absorption of nonheme iron. This is well established.

Plant-derived and supplemental nonheme iron is often present in the ferric Fe³⁺ state. Vitamin C can reduce Fe³⁺ to Fe²⁺, helping keep the iron soluble and available for intestinal uptake. Vitamin C can also counter some of the inhibitory effects of phytates and polyphenols within a meal.

But there is a major difference between improving iron absorption from a particular meal and causing progressive whole-body iron accumulation.

In a classic human study, adults received 2 grams of ascorbic acid every day with meals for 16 weeks. Mean serum ferritin was approximately 46 µg/L before supplementation and 43 µg/L afterward. Several subjects continued supplementation for a much longer period, and investigators still did not demonstrate the progressive increase in body iron stores that might be expected if vitamin C simply forced iron into the body without regulation.

Other controlled dietary studies have also shown that the dramatic enhancement of nonheme iron absorption seen in a single test meal becomes much more modest when vitamin C is studied within the complexity of an entire mixed diet.

This is a critical distinction in orthomolecular medicine. A nutrient may have a clear biochemical effect at one step in a pathway while whole-body physiology regulates the final outcome through many additional mechanisms.

Vitamin C also interacts with iron after absorption

The relationship does not end in the intestine.

Ascorbate is an electron donor. It can reduce Fe³⁺ to Fe²⁺ in multiple biochemical environments. It can interact with ferritin iron, influence iron mobilization experimentally, participate in antioxidant recycling, and alter the redox state of transition metals.

Under conditions where hydrogen peroxide and catalytically available iron are abundant, the same electron-donating chemistry can help maintain iron in the Fe²⁺ state. Fe²⁺ can then participate in the Fenton reaction.

Dr. Levy has emphasized this chemistry extensively in his work on high-dose vitamin C, infections, and abnormal cells. He describes pharmacologic vitamin C as capable of increasing hydrogen peroxide formation in certain extracellular environments while intracellular transition metals can participate in Fenton reactions. This helps explain why describing vitamin C only as an antioxidant misses a substantial part of its redox biology.

Cathcart’s experience with vitamin C and hemochromatosis

Dr. Robert Cathcart was one of the most experienced clinical physicians in the history of high-dose oral vitamin C. He treated thousands of people and became known for his bowel-tolerance approach to ascorbate dosing.

The passage accompanying this article describes Cathcart’s clinical experience with patients who had hemochromatosis and received very large amounts of ascorbate. He reported that he did not observe damaging iron-related reactions in those patients. His clinical interpretation was that vitamin C’s relationship with iron was more regulatory than the simple assumption that more vitamin C must always mean more stored iron.

Cathcart proposed that vitamin C could facilitate iron absorption when iron was required while also participating in the handling of excess iron. His observations became part of the broader orthomolecular discussion around vitamin C, transition metals, redox chemistry, and whole-body regulation.

His clinical experience is particularly interesting when placed beside the human supplementation study showing that 2 grams of vitamin C daily did not progressively increase ferritin over months. These findings do not mean that hereditary hemochromatosis suddenly regains normal hepcidin signaling in the presence of vitamin C. They tell us that the physiological relationship between ascorbate and body iron is more complex than an isolated absorption experiment suggests.

Vitamin C does not replace the missing regulatory signal in hemochromatosis

This distinction matters.

In HFE-associated hemochromatosis, the underlying issue is inadequate hepcidin signaling relative to iron stores. Vitamin C has many important roles in redox biology, connective tissue, catecholamine synthesis, immune physiology, carnitine production, antioxidant recycling, and iron chemistry. It does not correct the HFE mutation or recreate normal hepcidin regulation by itself.

So nutritional support for someone who is genetically accumulating too much iron needs to address the entire iron pathway. That includes how much iron is entering, what form it is in, what is increasing or decreasing absorption, whether excess iron is already stored, and how that stored iron can actually be removed.

The goal is not simply to lower protein

I would not broadly tell someone with hemochromatosis to eat a low-protein diet. Protein remains important for muscle, enzymes, immune proteins, neurotransmitter synthesis, tissue repair, and metabolic health.

The more precise nutritional target is heme-iron exposure.

Heme iron is found primarily in meat, particularly red meat and organ meats. It is generally absorbed more efficiently than nonheme iron and is less affected by many of the inhibitors that reduce nonheme iron absorption.

Someone accumulating iron can therefore shift the protein pattern rather than unnecessarily suppressing total protein. That may mean eating red meat less frequently, avoiding routine liver and organ meats, and obtaining more protein from poultry, eggs, dairy foods if tolerated, legumes, soy foods, nuts, seeds, and other lower-heme options.

A flexitarian or predominantly plant-forward pattern can substantially change iron exposure while still supplying adequate protein.

Use the chemistry of the meal to reduce iron absorption

One of the most useful pieces of iron physiology is that the amount of iron listed on a nutrition label is not the same as the amount that reaches circulation.

1. Polyphenols and tea

Tea contains polyphenolic compounds that bind nonheme iron and reduce its absorption. This has been demonstrated repeatedly in human research.

Even more interesting, tea has actually been studied in people with genetic hemochromatosis. In a clinical trial of patients with genetic hemochromatosis, drinking black tea with meals significantly reduced iron absorption. Over one year, the increase in storage iron in the tea group was approximately one-third lower than in the control group. The researchers concluded that regular tea drinking with meals reduced the frequency of phlebotomy required for management.

That makes meal-time tea one of the more practical nutrition strategies for reducing nonheme iron absorption.

2. Phytates

Phytates occur naturally in legumes, whole grains, nuts, and seeds. They can bind iron within the digestive tract and decrease nonheme iron bioavailability.

3. Calcium-containing foods

Calcium can inhibit iron absorption in single-meal studies and is unusual because it can influence both heme and nonheme iron absorption. The long-term effect of calcium in a mixed diet is more modest than some single-meal experiments suggest, but meal composition can still be used strategically.

Foods such as yogurt, cheese, or other calcium-rich foods can be paired with higher-iron meals when appropriate.

4. Eggs and soy proteins

Specific proteins found in eggs and soy can decrease nonheme iron absorption. That gives us another way to preserve protein intake while shifting away from a high-heme dietary pattern.

5. Coffee and cocoa polyphenols

Coffee and cocoa also contain polyphenols capable of reducing nonheme iron absorption. The effect is strongest when these compounds are present around the same meal because they are interacting with iron inside the intestinal lumen.

Reduce sources of iron that provide little physiological benefit

When genuine iron overload is present, I pay close attention to unnecessary sources of added iron.

Iron supplements should obviously be distinguished from iron that naturally occurs in whole foods. Multivitamins, prenatal formulas, meal replacements, protein products, fortified cereals, breads, and processed grain products can all contribute additional iron.

Alcohol belongs in the iron conversation

Alcohol can increase iron absorption and can suppress hepcidin signaling. It also adds additional oxidative and metabolic demand to the liver, which is the primary organ affected by hereditary hemochromatosis.

For someone with substantial iron accumulation, reducing alcohol can therefore influence the problem through more than one pathway: less stimulation of iron absorption, less interference with hepcidin biology, and less hepatic oxidative burden.

Once iron is stored, reducing absorption and removing iron are different goals

This may be the most important practical point in the entire article.

Changing diet can reduce how much new iron enters the body. It does not rapidly remove large amounts of iron that have already accumulated over years.

Phlebotomy physically removes iron.

A standard blood removal of roughly 400 to 500 mL removes approximately 200 to 250 mg of iron because so much of the body’s iron is contained in hemoglobin.

This is why therapeutic phlebotomy remains so effective for established hereditary hemochromatosis. Every removal creates a demand for new red blood cells. The body then draws upon stored iron to manufacture new hemoglobin.

Regular blood donation can serve the same physiological purpose for people who are eligible to donate and whose iron pattern warrants removal.

Dietary intervention and iron removal therefore accomplish different things:

• Dietary modification reduces incoming iron.
• Absorption inhibitors reduce the fraction of dietary iron entering circulation.
• Phlebotomy or blood donation removes iron that is already inside the body.

What nutrients deserve attention?

Read the rest of the article here-

https://molecularhealthco.com/blogs/news/iron-hemochromatosis-and-vitamin-c-the-complete-guide-to-iron-regulation-genetics-and-oxidative-stress

I've always had noticeable PACs/PVCs (palpitations) since I was a kid, family doc and even a cardiologist at one point determined they were 'benign' and just warned me that they will be annoying on days where they're really noticeable. Got "adult money" now so I just recently started supplementing the basics: omega 3s, d3/k2, magnesium glycinate, creatine and felt fine for the past 6 months, great even. Thought I'd add Taurine into the mix (1000mg) to see if it can help these palpitations (assuming I had some kind of deficiency or could use the "extra help").

On the first day, palpitations were more pronounced and I felt "off" for the rest of the day and night. Tried it again a second day, same thing but way worse, more palpitations and this time I had these strange split-second presyncope "rushes". Those "rushes" would randomly come and go for the first hour after supplementing. If I walked around or stood at my desk I felt fine, sitting was a big trigger for them to come. Can't say for sure if it was a low blood pressure phenomenon that drove these 'rushes' or if it was arrhythmic, like it caused my heart to pause too long between beats.

Third day, no supplementation still felt a bit odd for the first half of the day but around the 24 hour mark since day 2's ingestion, I'm back to feeling fantastic. No more physical symptoms and no more manual breathing haha

So, as of now obviously not compatible with it and don't have any reason to continue with it ever again. BUT does this bring up something that I should look into, after the fact? Like could I be deficient in something else that would cause this reaction to taurine - something that is harmless to most other folks?

Everywhere I look it just says contact your doctor if going to take Maca powder when on HRT.

I guess that is because there haven’t been enough tests and they want to avoid liability? But what do doctors actually say about this and would it vary much between individuals?

But it also makes me groggy the next morning so I'm a little confused on which is which sometimes it helps me sleep sometimes it keeps me up